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The self-correction program of the US Internal Revenue Service for corporate pension plans ensures compliance with changes in the Employee Retirement Income Security Act of 1974 and the avoidance of penalties for employers and plan trustees.

This article describes some of the problems within the Employee Retirement Income Security Act of 1974 (ERISA). The significance of such problems become glaring in light of the recent malfeasance by Enron, and Anderson. The two most significant problems appear to be that the law does not require that the company employee (usually an executive) overseeing the company's 401 (K) plan does not have to be legal, investment, or administrative experience.

This article provides an overview of the Department of Labor's new Voluntary Fiduciary Correction (VFC) Program. The VFC Program is designed to allow fiduciaries, plan sponsors, parties-in-interest, and any other persons in a position to correct a breach of fiduciary responsibilities may correct such problems by filing an application with the DOL. In some cases this could mean no legal action would be taken regarding the correction. However, restrictions exist.

This article describes the severity of businesses failing to comply with the IRS CAP regulations, and offers suggestions to companies for dealing with the failure without incurring monetary sanctions that can otherwise be quite substantial.

Methotrexate was originally used as an anticancer agent, but has more recently become useful in the treatment of rheumatoid arthritis. The drug is effective against cancerous cells because it prevents use by the cells of methyl groups (single-carbon compounds), donated by folic acid and important in the production of DNA and other compounds. The mechanism by which methotrexate modulates the inflammatory and other processes of rheumatoid arthritis is not known. Differing effects on immune cell functions have been reported. Several slow-acting antirheumatic drugs are known to modulate the function of monocytes, a type of white blood cell important in many chronic inflammatory disorders, but the effects of methotrexate on these cells has not been well studied. The effects of the drug on monocytes from healthy donors were evaluated. Monocytes are important in the body's reactions to cell damage or infection. Methotrexate inhibited two monocyte functions important in these reactions, chemotaxis (migration to foreign cells or damaged sites, guided by chemical attractants) and production of superoxide (a form of oxygen important in fighting foreign cells), and this inhibition was time- and dose-dependent. Folinic acid, the active form of folic acid, reversed the inhibitory effects of methotrexate. Effects of methotrexate were boosted by using culture medium (the solution used to support monocyte survival outside the body) that was low in methionine (a protein component that also is used in reactions to supply methyl groups), and this could be reversed by addition of methionine or of S-adenosylmethionine, a major methyl group donor. The study suggests that methotrexate probably exerts its anti-inflammatory effects by blocking methylation-dependent reactions that occur during inflammatory reactions. (Consumer Summary produced by Reliance Medical Information, Inc.)

Some infectious and inflammatory disorders cause increased blood levels of rheumatoid factors (RFs), antibodies (immunoglobulins, Igs) that recognize and attack a part of the protein structure that is common to one subtype of Igs, the IgG class. In some diseases, the increased levels of RFs are reversible, while the elevations occurring in rheumatoid arthritis and juvenile rheumatoid arthritis are chronic and usually irreversible. The factors responsible for elevated RFs in these rheumatic diseases are uncertain. RFs are produced by B cells or lymphocytes, a type of white blood cell involved in immune function, and some studies suggest that a particular type of RF, IgM RF, may contribute to RF production by activating B cells. The effect of IgM RF on B cell activity was studied using RF obtained from the blood of nine female patients with juvenile rheumatoid arthritis. The levels of IgM RF from the patients strongly correlated with production of IgM RF by lymphocytes isolated from healthy adults. Nonspecific stimulation of lymphocytes by other techniques also caused IgM production, but much less IgM RF activity was present. In addition, lymphocytes stimulated with IgM RF also produced IgG, and this correlated with the levels of IgM RF. The results suggest that once IgM RF is produced, it can further increase IgM RF production by B lymphocytes, and this may contribute to the chronic production of RF in juvenile rheumatoid arthritis. (Consumer Summary produced by Reliance Medical Information, Inc.)